Oxidative　damage　is　an　important　mediator　of　Alzheimer＇s　disease　(AD);　hence,　antioxidant　therapy　is　a　potential　treatment　for　AD.　Edaravone,　a　free　radical　scavenger,　has　been　shown　to　have　neuroprotective　properties.　The　study　aimed　to　examine　the　effects　of　edaravone　on　indicators　of　A　beta　25-35-induced　oxidative　damage　in　PC12　cells.　PC12　cells　were　treated　with　20,　40,　or　80　mu　M　edaravone　before　treatment　with　30　mu　M　A　beta　25-35.　After　treatment,　the　following　assessments　were　performed:　cell　viability　and　aggregation,　oxidative　stress,　mitochondrial　peroxidation,　generation　of　reactive　oxygen　species　(ROS),　and　apoptosis.　Aggregation,　lactate　dehydrogenase　activity,　malondialdehyde　concentrations,　mitochondrial　peroxidation,　ROS　levels,　and　apoptosis　were　significantly　increased　in　A　beta　25-35-treated　cells　but　decreased　in　the　treatment　with　edaravone　40　and　80　mu　M.　In　contrast,　intracellular　glutathione　and　superoxide　dismutase　concentrations　were　significantly　decreased　in　A　beta　25-35-treated　cells　but　increased　in　the　treatment　with　edaravone　40　and　80　mu　M.　Edaravone　ameliorates　oxidative　damage　associated　with　A　beta　25-35　treatment　in　PC12　cells.　Our　findings　support　the　continued　investigation　of　edaravone　as　a　potential　treatment　for　AD.